TY - JOUR
T1 - TRL, IDL, and LDL Apolipoprotein B-100 and HDL Apolipoprotein A-I Kinetics as a Function of Age and Menopausal Status
AU - Matthan, N.R.
AU - Jalbert, S.M.
AU - Lamon-Fava, S.
AU - Dolnikowski, G.G.
AU - Welty, F.K.
AU - Barrett, Hugh
AU - Schaefer, E.J.
AU - Lichtenstein, A.H.
PY - 2005
Y1 - 2005
N2 - Objective - To determine mechanisms contributing to the altered lipoprotein profile associated with aging and menopause, apolipoprotein B- 100 ( apoB- 100) and apoA- I kinetic behavior was assessed.Methods and Results - Eight premenopausal ( 25 +/- 3 years) and 16 postmenopausal ( 65 +/- 6 years) women consumed for 6 weeks a standardized Western diet, at the end of which a primed- constant infusion of deuterated leucine was administered in the fed state to determine the kinetic behavior of triglyceride- rich lipoprotein ( TRL), intermediate-density lipoprotein ( IDL), and low- density lipoprotein ( LDL) apoB- 100, and high- density lipoprotein ( HDL) apoA- I. Data were fit to a multicompartmental model using SAAM II to calculate fractional catabolic rate ( FCR) and production rate ( PR). Total cholesterol, LDL cholesterol ( LDL- C), TRL- C, and triglyceride levels were higher ( 50%, 55%, 130%, and 232%, respectively) in the postmenopausal compared with the premenopausal women, whereas HDL- C levels were similar. Plasma TRL, IDL, and LDL - apoB- 100 levels and pool sizes ( PS) were significantly higher in the postmenopausal than premenopausal women. These differences were accounted for by lower TRL, IDL, and LDL apoB- 100 FCR ( P < 0.05), with no difference in PR. There was no significant difference between groups in HDL- C levels or apoA- I kinetic parameters. Plasma TRL- C concentrations were negatively correlated with TRL apoB- 100 FCR ( r = - 0.46; P < 0.05) and positively correlated with PR ( r = 0.62; P < 0.01). Plasma LDL- C concentrations were negatively correlated with LDL apoB- 100 FCR ( r = - 0.70; P < 0.001) but not PR.Conclusions - The mechanism for the increase in TRL and LDL apoB- 100 PS observed in the postmenopausal women was determined predominantly by decreased TRL and LDL catabolism rather than increased production. No differences were observed in HDL apoA- I kinetics between groups.
AB - Objective - To determine mechanisms contributing to the altered lipoprotein profile associated with aging and menopause, apolipoprotein B- 100 ( apoB- 100) and apoA- I kinetic behavior was assessed.Methods and Results - Eight premenopausal ( 25 +/- 3 years) and 16 postmenopausal ( 65 +/- 6 years) women consumed for 6 weeks a standardized Western diet, at the end of which a primed- constant infusion of deuterated leucine was administered in the fed state to determine the kinetic behavior of triglyceride- rich lipoprotein ( TRL), intermediate-density lipoprotein ( IDL), and low- density lipoprotein ( LDL) apoB- 100, and high- density lipoprotein ( HDL) apoA- I. Data were fit to a multicompartmental model using SAAM II to calculate fractional catabolic rate ( FCR) and production rate ( PR). Total cholesterol, LDL cholesterol ( LDL- C), TRL- C, and triglyceride levels were higher ( 50%, 55%, 130%, and 232%, respectively) in the postmenopausal compared with the premenopausal women, whereas HDL- C levels were similar. Plasma TRL, IDL, and LDL - apoB- 100 levels and pool sizes ( PS) were significantly higher in the postmenopausal than premenopausal women. These differences were accounted for by lower TRL, IDL, and LDL apoB- 100 FCR ( P < 0.05), with no difference in PR. There was no significant difference between groups in HDL- C levels or apoA- I kinetic parameters. Plasma TRL- C concentrations were negatively correlated with TRL apoB- 100 FCR ( r = - 0.46; P < 0.05) and positively correlated with PR ( r = 0.62; P < 0.01). Plasma LDL- C concentrations were negatively correlated with LDL apoB- 100 FCR ( r = - 0.70; P < 0.001) but not PR.Conclusions - The mechanism for the increase in TRL and LDL apoB- 100 PS observed in the postmenopausal women was determined predominantly by decreased TRL and LDL catabolism rather than increased production. No differences were observed in HDL apoA- I kinetics between groups.
U2 - 10.1161/01.ATV.0000172629.12846.b8
DO - 10.1161/01.ATV.0000172629.12846.b8
M3 - Article
SN - 1079-5642
VL - 25
SP - 1691
EP - 1696
JO - Arteriosclerosis, thrombosis, and vascular biology
JF - Arteriosclerosis, thrombosis, and vascular biology
IS - 8
ER -